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  • Open Access

    ARTICLE

    MicroRNA-520b Functions as a Tumor Suppressor in Colorectal Cancer by Inhibiting Defective in Cullin Neddylation 1 Domain Containing 1 (DCUN1D1)

    Jing Xiao*, Guang Li, Jingyu Zhou, Shalong Wang, Dongcai Liu, Guoshun Shu, Jianping Zhou, Feng Ren

    Oncology Research, Vol.26, No.4, pp. 593-604, 2018, DOI:10.3727/096504017X14920318811712

    Abstract MicroRNAs (miRs), a class of small noncoding RNAs, are important regulators for gene expression through directly binding to the 3'-untranslated region (3'-UTR) of their target mRNA. Recently, downregulation of miR-520b has been observed in several common human cancers. However, the exact role of miR-520b in colorectal cancer (CRC) has not previously been studied. In this study, our data showed that miR-520b was significantly downregulated in CRC and cell lines when compared with adjacent normal tissues and a normal intestinal epithelial cell line. Low expression of miR-520b was notably associated with the malignant progress and a… More >

  • Open Access

    ARTICLE

    Overexpression of Glypican 5 (GPC5) Inhibits Prostate Cancer Cell Proliferation and Invasion via Suppressing Sp1-Mediated EMT and Activation of Wnt/β-Catenin Signaling

    Yu Sun1, Kai Xu1, Miao He, Guilian Fan, Hongming Lu

    Oncology Research, Vol.26, No.4, pp. 565-572, 2018, DOI:10.3727/096504017X15044461944385

    Abstract Glypican 5 (GPC5) belongs to the family of heparan sulfate proteoglycans (HSPGs). It was initially known as a regulator of growth factors and morphogens. Recently, there have been reports on its correlation with the tumorigenic process in the development of some cancers. However, little is known about its precise role in prostate cancer (PCa). In the present study, we explored the expression pattern and biological functions of GPC5 in PCa cells. Our results showed that GPC5 was lowly expressed in PCa cell lines. Upregulation of GPC5 significantly inhibited PCa cell proliferation and invasion in vitro More >

  • Open Access

    ARTICLE

    Tanshinone Suppresses Arecoline-Induced Epithelial–Mesenchymal Transition in Oral Submucous Fibrosis by Epigenetically Reactivating the p53 Pathway

    Lian Zheng, Zhen-Jie Guan, Wen-Ting Pan, Tian-Feng Du, Yu-Jia Zhai, Jia Guo

    Oncology Research, Vol.26, No.3, pp. 483-494, 2018, DOI:10.3727/096504017X14941825760362

    Abstract Oral submucous fibrosis (OSF) induced by chewing of the areca nut has been considered to be a precancerous lesion with a high probability of developing oral squamous cell carcinoma. Tanshinone (TSN) is the main component extracted from Salvia miltiorrhiza, a traditional Chinese medicine, which was found to have diverse pharmacological effects, such as anti-inflammatory and antitumor. In the current study, we aimed to identify the inhibitory effects and the underlying mechanism of TSN on OSF progress. We found that treatment with TSN inhibited the arecoline-mediated proliferation of primary human oral mucosal fibroblasts and reversed the… More >

  • Open Access

    ARTICLE

    MicroRNA-138 Inhibits Cell Growth, Invasion, and EMT of Non-Small Cell Lung Cancer via SOX4/p53 Feedback Loop

    Dandan Li*, Changjun He, Junfeng Wang, Yanbo Wang, Jianlong Bu, Xianglong Kong, Dawei Sun

    Oncology Research, Vol.26, No.3, pp. 385-400, 2018, DOI:10.3727/096504017X14973124850905

    Abstract Many studies have shown that downregulation of miR-138 occurs in a variety of cancers including non-small cell lung cancer (NSCLC). However, the precise mechanisms of miR-138 in NSCLC have not been well clarified. In this study, we investigated the biological functions and molecular mechanisms of miR-138 in NSCLC cell lines, discussing whether it could turn out to be a therapeutic biomarker of NSCLC in the future. In our study, we found that miR-138 is downregulated in NSCLC tissues and cell lines. Moreover, the low level of miR-138 was associated with increased expression of SOX4 in… More >

  • Open Access

    ARTICLE

    miR-644a Inhibits Cellular Proliferation and Invasion via Suppression of CtBP1 in Gastric Cancer Cells

    Yingchao Li*, Xiaoni Yan*, Li Ren*, Yang Li

    Oncology Research, Vol.26, No.1, pp. 1-8, 2018, DOI:10.3727/096504016X14772410356982

    Abstract Epithelial–mesenchymal transition (EMT) is one of the most important mechanisms in the metastasis of various cancers, including gastric cancer (GC). In this study, we explored the putative significance of miR-644a and its role in EMT-mediated metastasis of GC. We first detected the expression of miR-644a in a cohort of 107 GC tissues using quantitative RT-PCR. The expression of miR-644a was suppressed in GC tissues and was associated with a later clinical stage and tumor metastasis. Restoring the expression of miR-644a could significantly suppress the migration and invasion of HGC-27 and SGC-7901 cells, which might be More >

  • Open Access

    ARTICLE

    Inhibition of ERK1/2 Signaling Impairs the Promoting Effects of TGF-β1 on Hepatocellular Carcinoma Cell Invasion and Epithelial–Mesenchymal Transition

    Ling Liu, Nianfeng Li, Qi Zhang, Jixiang Zhou, Ling Lin, Xinxin He

    Oncology Research, Vol.25, No.9, pp. 1607-1616, 2017, DOI:10.3727/096504017X14938093512742

    Abstract Transforming growth factor-b (TGF-β) and ERK signaling have been implicated in various human cancers including hepatocellular carcinoma, but the underlying mechanism remains largely unclear. In this study, we aimed to explore the role of ERK1/2 in the regulation of TGF-β’s promoting and suppressive activities in HCC cells. Our data showed that treatment with TGF-β1 enhanced invasion and epithelial–mesenchymal transition (EMT) in HCC HepG2 cells, accompanied with increased MMP9 production and activation of Smad2/3 and ERK1/2, but inhibited tumor cell proliferation. These effects were eliminated by treatment with SB431542, a TGF-β inhibitor. Afterward, treatment with the… More >

  • Open Access

    ARTICLE

    TRAF4 Regulates Migration, Invasion, and Epithelial–Mesenchymal Transition via PI3K/AKT Signaling in Hepatocellular Carcinoma

    Kairui Liu*, Xiaolin Wu*, Xian Zang, Zejian Huang*, Zeyu Lin, Wenliang Tan*, Xiang Wu*, Wenrou Hu*, Baoqi Li*, Lei Zhang*

    Oncology Research, Vol.25, No.8, pp. 1329-1340, 2017, DOI:10.3727/096504017X14876227286564

    Abstract Overexpression of the tumor necrosis factor receptor-associated factor 4 (TRAF4) has been detected in many cancer types and is considered to foster tumor progression. However, the role of TRAF4 in hepatocellular carcinoma (HCC) remains elusive. In this study, we found that TRAF4 was highly expressed in HCC cell lines and HCC tissues compared with normal liver cell lines and adjacent noncancerous tissues. TRAF4 overexpression in HCC tissues was correlated with tumor quantity and vascular invasion. In vitro studies showed that TRAF4 was associated with HCC cell migration and invasion. An in vivo study verified that More >

  • Open Access

    ARTICLE

    Upregulation of CD147 Promotes Metastasis of Cholangiocarcinoma by Modulating the Epithelial-to-Mesenchymal Transitional Process

    Paweena Dana*†‡, Ryusho Kariya, KulthidaVaeteewoottacharn*†, Kanlayanee Sawanyawisuth*†, Wunchana Seubwai†§, Kouki Matsuda, Seiji Okada, Sopit Wongkham*†

    Oncology Research, Vol.25, No.7, pp. 1047-1059, 2017, DOI:10.3727/096504016X14813899000565

    Abstract CD147 is a transmembrane protein that can induce the expression and activity of matrix metalloproteinases (MMPs). Expression of CD147 has been shown to potentiate cell migration, invasion, and metastasis of cancer. In this study, the critical role of CD147 in metastasis was elucidated using CD147-overexpressing cholangiocarcinoma (CCA) cells in vitro and in vivo. The molecular mechanism, demonstrated herein, supported the hypothesis that metastasis increased in CD147-overexpressing cells. Five CD147-overexpressing clones (Ex-CD147) were established from a low CD147-expressing CCA cell line, KKU-055, using lentivirus containing pReceiver-Lenti-CD147. The metastatic capability was determined using the tail vein injection… More >

  • Open Access

    ARTICLE

    Knockdown of Long Noncoding RNA CCAT2 Inhibits Cellular Proliferation, Invasion, and Epithelial–Mesenchymal Transition in Glioma Cells

    Jing Zeng*1, Tianping Du†1, Yafeng Song, Yan Gao, Fuyan Li, Ruimin Wu, Yijia Chen, Wei Li, Hong Zhou, Yi Yang, Zhijun Pei

    Oncology Research, Vol.25, No.6, pp. 913-921, 2017, DOI:10.3727/096504016X14792098307036

    Abstract Long noncoding RNA (lncRNA) colon cancer-associated transcript 2 (CCAT2) has been demonstrated to play an important role in diverse tumorigenesis. However, the biological function of lncRNAs in glioma is still unknown. In this study, we found that lncRNA CCAT2 was overexpressed in glioma tissues and cell lines and associated with tumor grade and size. Furthermore, patients with high levels of lncRNA CCAT2 had poorer survival than those with lower levels of lncRNA CCAT2. Knocking down lncRNA CCAT2 expression significantly suppressed the glioma cell growth, migration, and invasion, as well as induced early apoptosis of glioma More >

  • Open Access

    ARTICLE

    Silencing of A-Kinase Anchor Protein 4 (AKAP4) Inhibits Proliferation and Progression of Thyroid Cancer

    Jiakai Han1, Wei Gao1, Dongyue Su, Yang Liu

    Oncology Research, Vol.25, No.6, pp. 873-878, 2017, DOI:10.3727/096504016X14783701102564

    Abstract A-kinase anchor protein 4 (AKAP4), a member of the A-kinase anchor family of proteins, plays a role in tumor development and progression. However, its expression pattern and function in human thyroid cancer remain obscure. Here we examined AKAP4 expression in thyroid cancer cell lines as well as the effects of AKAP4 on the proliferation and metastasis of thyroid cancer cells. We also explored the molecular mechanism by which AKAP4 mediates the metastatic potential of thyroid cancer cells. Our results revealed that the transcript and protein levels of AKAP4 were significantly upregulated in thyroid cancer cell… More >

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